Following an intraperitoneal injection of acetaminophen into polycyclic hydrocarbon-responsive mice in which hepatic aryl hydrocarbon hydroxylase (AHH) activity has been induced by pretreatment with polycyclic hydrocarbons, lenticular opacification develops in a few hours. The opacity consists of a thin layer anterior to the equatorial cortex. Acetaminophen metabolites bind to the lens but do not lower the glutathione level. These observations suggest that lenticular opacification may be caused by binding of acetaminophen metabolites to the lens cells in the anterior portion and thus disrupting permeability properties of the cells. Since lenticular opacification develops when mice are pretreated with 3-methylcholanthrene (cytochrome P1 450 inducer) but not with phenobarbital (cytochrome P 450 inducer), acetaminophen metabolites that affect the lens must be produced by the cytochrome P1 450-dependent AHH system. BIBLIOGRAPHIC REFERENCE: Shichi, H., Tsunematsu, Y., and Nebert, D.W.: Aryl hydrocarbon hydroxylase induction in retinal pigmented epithelium: Possible association of genetic differences in a drug metabolizing enzyme with retinal degeneration. Exp. Eye Res. 23: 165-176, 1976.